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Am J Physiol Endocrinol Metab 276: E650-E657, 1999;
0193-1849/99 $5.00
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Vol. 276, Issue 4, E650-E657, April 1999

Plasma leptin levels and triglyceride secretion rates in VMH-lesioned obese rats: a role of adiposity

Asako Suga1,2, Tsutomu Hirano1, Shuji Inoue2, Masatomi Tsuji1, Toshimasa Osaka2, Yoshio Namba2, Masakazu Miura3, and Mitsuru Adachi1

1 First Department of Internal Medicine, Showa University School of Medicine, 2 Division of Geriatric Health and Nutrition, National Institute of Health and Nutrition, and 3 Mitsubishi Kagaku Bio-Clinical Laboratory, Tokyo 142-8666, Japan

To explore the role of adiposity on hypertriglyceridemia associated with obesity, we examined the relation between triglyceride secretion rate (TGSR) and plasma leptin, insulin, or insulin resistance in ventromedial hypothalamus (VMH)-lesioned rats in the dynamic and static phases (2 and 14 wk after lesions, respectively). VMH-lesioned rats gained body weight (BW) at fivefold higher rates in the dynamic phase compared with sham-operated control (sham) rats, and BW gain reached a plateau in the static phase. Parametrial fat pad mass was increased 2.5-fold in VMH-lesioned rats compared with sham rats in both phases. Leptin levels were sixfold higher in VMH-lesioned rats of the dynamic phase and even higher in the static phase. Insulin levels were twofold higher in VMH-lesioned rats than in sham rats in both phases. In the dynamic phase, VMH-lesioned rats had 2-fold higher plasma triglyceride (TG) levels and 2.6-fold higher TGSRs, whereas steady-state plasma glucose (SSPG) values, an indicator of insulin resistance, were lower. SSPG values became significantly higher in VMH-lesioned rats in the static phase, but TGSR was not further accelerated. TGSR was significantly associated with leptin, independent of insulin. Leptin was highly correlated with BW, fat mass, and nonesterified fatty acids (NEFA). These results suggest that adiposity itself plays a critical role in TGSR probably through increased NEFA flux from enlarged adipose tissues. Insulin resistance is not associated with the overproduction of TG in this animal model for obesity.

hyperinsulinemia; insulin resistance; ventromedial hypothalamus lesions


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